Susan Desmond-Hellmann
speaker
362 appearances
1 recordings
1 series
first heard Apr 2025
last heard Apr 2025
Susan Desmond-Hellmann’s voice in public audio — every appearance, attributed to the second.
Trend
recordings per month · last 12 monthsNo recordings in the last 12 months.Older appearances are listed below; set an alert to hear about the next one.
Appearances
They had those three drugs. They had growth hormone, TPA, and palmozyme.
I think they needed the money.
I don't think they have the scope to even make it.
Oh, yeah. Yeah, for sure it was the opportunity. I will tell you, if you were me in 1995, sitting down with Art Levinson, and he was the head of research then, and he was talking about the future and oncology, what the plans were, you'd have gone too. Yeah. You got to. For sure, it was an opportunity. We were doing well.
I will say that further down on the list of pros and cons was West Coast is home. I mean, Connecticut was snowy and cold. I didn't come over on the Mayflower, it turns out. I mean, I loved people at Bristol-Myers Squibb. I loved the job. And I loved being in San Francisco. Yeah, that was a big deal. But I believed Art when he said we're going to be a cancer company.
Ah, thrombopoietin. They hired me to work on thrombopoietin. It was going to be the third leg of the stool. EPO, so make your red cells go up, neupogen for your white cells, and TPO for your platelets. And it was a big race. Amgen was in the race.
Yeah, EPO and neupogen.
Amgen and Genentech had always been kind of rivals. And when they cloned thrombopoietin at Genentech, I read the paper and then they called me. Did I want to come work on it? It was that kind of thing.
It's a race.
So you patent it, then you publish, then you make the recombinant.
Mm-hmm. Genentech, one of their great assets started by Herb Boyer is they publish. They don't stop the scientists from publishing. They get the lawyers in there quick and they make sure that they protect the IP of the company, but they want people to publish. It's very academic.
So thrombopoietins, EPO and Neupogen are as if you design them to make recombinant forms and give them for cancer patients or other patients who need them. Thrombopoietin, not so much. To make it simple, if you said, okay, your platelets are going way down from your chemotherapy and I'm going to give you thrombopoietin to make them go up, they come back up really late and they go too high.
So I'm making you at risk for a blood clot by giving you a million platelets, but later than you need to and you're recovering on your own already.
Once we looked at how it worked in patients, we knew better than we had before. The kinetics of really recovering from not all chemotherapy, as you know, causes your platelets to go low.
Right, right. And this tricky thing about going too high, if you're wrong, it's a problem.
You could platelet-pherese them. I mean, there are remedies, but you don't want to do that. Anyway, so thrombopoietin proved to be very, very difficult drug. And I learned a lot about the cancer equivalent or the product development equivalent of tulip mania. Yeah. When everybody's so excited, you get excited too. And it's like, oh, I did learn a lot.
I've often reflected on what might happen that I'm not thinking about now. But what also happened is the labs at Genentech had been working on Herceptin, on Trastuzumab. For a while, Art became the CEO. Art Levinson became the CEO in 95. And he wanted to push on having trastuzumab, Herceptin, get into the clinic.
trastuzumab, or I'll call it Herceptin because it's less of a mouthful, is a antibody. Like you and I have antibodies that fight disease in our bodies. And it's an antibody that targets this protein called HER2. And HER2 matters because about one in four women with breast cancer have too much of it. And when you have too much of it, if you've got too much HER2 from the time you're diagnosed,
Your median average survival is three years. If you don't have too much of it, it's seven years. So you know what matters. So the concept with this antibody is turn that off. Whatever bad thing that drives it down to three years, turn that off and go back to seven years. Pretty simple concept.
The thesis was that it was telling the cell to grow. That it was giving a growth signal to the nucleus to say, grow more. And if you could shut that off, you'd grow less. Now, later, we armed Hercept and we put a payload on it. So then you could say, both change the grow more signal and you've got a little bomb on there.
Showing 121–140 of 362 · page 7 of 19
← Previous
Next →